During effortful unilateral contractions, muscle activation is not limited to the target muscles but activity is also observed in contralateral muscles. The amount of this associated activity is depressed in a fatigued muscle, even after correction for fatigue-related changes in maximal force. In the present experiments, we aimed to compare fatigue-related changes in associated activity vs. parameters that are used as markers for changes in central nervous system (CNS) excitability. Subjects performed brief maximal voluntary contractions (MVCs) with the index finger in abduction direction before and after fatiguing protocols. We followed changes in MVCs, associated activity, motor-evoked potentials (MEP; transcranial magnetic stimulation), maximal compound muscle potentials (M waves), and superimposed twitches (double pulse) for 20 min after the fatiguing protocols. During the fatiguing protocols, associated activity increased in contralateral muscles, whereas afterwards the associated force was reduced in the fatigued muscle. This force reduction was significantly larger than the decline in MVC. However, associated activity (force and electromyography) remained depressed for only 5-10 min, whereas the MVCs stayed depressed for over 20 min. These decreases were accompanied by a reduction in MEP, MVC electromyography activity, and voluntary activation in the fatigued muscle. According to these latter markers, the decrease in CNS motor excitability lasted much longer than the depression in associated activity. Differential effects of fatigue on (associated) submaximal vs. maximal contractions might contribute to these differences in postfatigue behavior. However, we cannot exclude differences in processes that are specific to either voluntary or to associated contractions.

The function and regulation of the myometrium, especially during pregnancy, labour and birth are important in reproductive physiology. It is crucial to understand the mechanisms that generate and modulate uterine contractility in order to be able to prevent and/or treat the problems related with the myometrium. A limited understanding of the cellular and molecular events underlying these phenomena complicates the situation. Various agonists, hormones, transmitters and/or chemicals are related to the regulation of the functions of the myometrium. Although notable advances regarding the key steps in receptor signalling explaining the actions of these factors have been achieved, a good deal of information is still necessary to understand this vital process. A better comprehension of myometrium physiology and the translation of research findings to clinical settings will help progress in women's health. In this review, we attempt to present a critical overview of myometrial functions and focus specifically on the role of calcium.

We used electrophysiological measures to investigate the effects of obstructive sleep apnea on attention, learning, and memory. Thirty subjects (OSA group, n = 15, control group n = 15) participated in n-back tests, accompanied by P300 recordings, to investigate working memory and attention. The mirror-drawing test was used to study procedural memory, and the trail-making test (TMT) was used to evaluate divided attention and executive function. No significant group difference in reaction time was found in the 0-back and 1-back tests. In the 2-back test, reaction times of patients were longer than those of the control group. No P300 wave was obtained in the OSA group in any (0-, 1-, or 2-back) n-back test. In contrast, in the control group, significant P300 waves were recorded except for the 2-back test. The mirror-drawing scores were unaffected by sleep apnea. There was no difference between groups in the TMT-A test on any of the trials. Although no group difference was found in the first or second trials of the TMT-B test, OSA patients were less successful in learning on the third trial. According to our study results, OSA affects attention and executive function adversely however, we could not detect a significant effect on working or procedural memory.

Our results indicate higher erythrocyte deformability and quicker erythrocyte aggregation in FM patients.

To investigate a possible relation between hypercholesterolemia and detrusor smooth muscle function, we studied the contractile response to potassium challenge, carbachol (CCh), and the components of CCh-induced contractile mechanism in high-cholesterol diet-fed rats. Adult male Sprague-Dawley rats were fed with standard (control group, N = 17) or 4 % cholesterol diet (hypercholesterolemia group (HC), N = 16) for 4 weeks. Spontaneous contractions of detrusor muscle strips and their responses to potassium chloride (KCl) or cumulative dose-contraction curves to CCh were recorded. The effects of muscarinic receptor antagonists (methoctramin and/or 4-diphenylacetoxy-N-methylpiperidine), L-type Ca(+2) channel blocker (nifedipine), and/or rho-kinase inhibitor Y-27632 were investigated. Blood cholesterol level was increased in the HC group with no sign of atherosclerosis. The KCl-induced detrusor smooth muscle contractions were higher in HC, whereas spontaneous and CCh-induced responses were similar in both groups. Preincubation with receptor antagonist for M(3) but not for M(2) attenuated contraction significantly, shifting the dose-response curve to the right. This response was similar in both groups. Among two effector mechanisms of M(3)-mediated detrusor smooth muscle contraction, rho-kinase pathway was not affected by hypercholesterolemia, whereas blockade of L-type Ca(+2) channels potently reduced contractions. The results of this study point out a relation between hypercholesterolemia and contractile mechanism of detrusor smooth muscle likely to change urinary bladder function, via altering L-type Ca(+2) channels. Taken together with escalating incidence of hypercholesterolemia and lower urinary tract symptoms, it is a field which deserves to be investigated further.

Background/Aims: We aimed to explore the immunological outcomes of short-term mental stress in apoptosis in peripheral lymphocytes and variations by gender and hormonal status of the individuals together with possible mediators of this interaction. Methods: Acute mental stress (computerized Stroop color-word interference and cold pressor tests) was applied to men (n = 17) and women (n = 16, in both follicular and luteal phases). Heart rate and blood pressure were monitored throughout the test and after the test until baseline values were recorded. Blood samples were drawn for measuring cortisol and nitric oxide (NO) levels and flow-cytometric cell counting before and after the test. Results: Activation of the stress system was ascertained by increased heart rate, blood pressure and serum cortisol levels after the test. Relative to baseline values, acute mental stress altered the distribution of T and natural killer cells. There was a significant decrease in T helper/T cytotoxic-suppressor cell ratio and an increase in apoptotic T helper cell percentage irrespective of gender or menstrual cycle phase. An increased number of natural killer cells was detected in women, whereas it was decreased in men. After stress induction, serum NO levels remained the same in women and increased in men. Although a correlation was not found between immune system changes and NO levels, glucocorticoids seem to have a role in the observed differences. Conclusion: Acute mental stress triggers apoptotic T helper cell loss which was associated with stress system activation, and sex steroids affect the pattern of stress-related immune cell distribution.

To evaluate the effects of hypercholesterolemia on the relaxation function of the urinary bladder, we examined the physiological mechanisms involved in the isoproterenol-induced relaxation in isolated detrusor strips in vitro and voiding behavior in vivo in rats. Adult male Sprague-Dawley rats were fed standard (control, N = 16) or 4 % cholesterol diet (hypercholesterolemia, N = 17) for 4 weeks. Concentration-response curves for isoproterenol-induced relaxations in carbachol-precontracted detrusor muscle strips were recorded. The contributions of β2- and β3-adrenoceptors and ATP-dependent and Ca(2+)-dependent potassium channels to the relaxation response were investigated by using selective adrenergic agonists salbutamol and BRL 37344 and specific potassium channel inhibitors glibenclamide and charybdotoxin, respectively. Cystometrography was performed to assess bladder function. Hypercholesterolemic rats had higher serum cholesterol and low- and high-density lipoprotein levels than the controls with no sign of atherosclerosis. Isoproterenol-induced relaxation was significantly enhanced in the hypercholesterolemia group. Preincubation with the M2 receptor antagonist attenuated the relaxation response in both groups. The relaxation responses to isoproterenol and salbutamol were similar in both groups, while BRL 37344 appeared to produce a greater relaxant effect in the hypercholesterolemic rats. Also, the inhibitory effects of potassium channel inhibitors on relaxation responses were comparable among the groups. The cystometric findings revealed that threshold and basal pressure values were higher in the hypercholesterolemia group compared with controls. We showed that hypercholesterolemia leads to greater relaxation responses to isoproterenol, appears to impair the braking function of M2 cholinergic receptors on adrenoceptor-induced relaxations in the isolated detrusor muscle, and affects the voiding function in rats.

The findings of this study show that transient hypotension induces a kidney injury in pregnant rats. MDA and GSH in kidneys seem to play a role in the pathophysiology of this injury. However, the roles of antioxidant enzymes and NO and the other underlying mechanisms deserve and necessitate further investigation regarding the long-term health of the mother and fetus.